The carotid body functions as a sensor: it responds to a stimulus, primarily O2 partial pressure, which is detected by the type I (glomus) cells, and triggers an action potential through the afferent fibers of the glossopharyngeal nerve, which relays the information to the central nervous system.

[5] The output of the carotid bodies is low at an oxygen partial pressure above about 100mmHg (13,3 kPa) (at normal physiological pH), but below 60mmHg the activity of the type I (glomus) cells increases rapidly due to a decrease in hemoglobin-oxygen saturation below 90%.

Other theories suggest it may involve mitochondrial oxygen sensors and the haem-containing cytochromes that undergo reversible one-electron reduction during oxidative-phosphorylation.

In normoxia, haem-oxygenase generates carbon monoxide (CO), CO activates the large conductance calcium-activated potassium channel, BK.

AMPK has a number of targets and it appears that, in the carotid body, when AMPK is activated by hypoxia, it leads to downstream potassium channel closure of both O2-sentive TASK-like and BK channels[10] An increased PCO2 is detected because the CO2 diffuses into the cell, where it increases the concentration of carbonic acid and thus protons.

Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in PCO2 sensing.

This causes exocytosis of vesicles containing a variety of neurotransmitters, including acetylcholine, noradrenaline, dopamine, adenosine, ATP, substance P, and met-enkephalin.

These act on receptors on the afferent nerve fibres which lie in apposition to the glomus cell to cause an action potential.

The feedback from the carotid body is sent to the cardiorespiratory centers in the medulla oblongata via the afferent branches of the glossopharyngeal nerve.